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Ecotropic viral integration site 5

EVI5, neuroblastoma stage 4S, NB4S
Top mentioned proteins: SET, CAN, DRB1, Epidermodysplasia Verruciformis, CLEC16A
Papers on EVI5
A non-synonymous single-nucleotide polymorphism associated with multiple sclerosis risk affects the EVI5 interactome.
Oksenberg et al., San Francisco, United States. In Hum Mol Genet, Jan 2016
Here, we have identified through fine mapping and meta-analysis EVI5 as the most plausible disease risk gene within the 1p22.1 locus.
Distinct differences in global gene expression profiles in non-implanted blastocysts and blastocysts resulting in live birth.
Lykke-Hartmann et al., Århus, Denmark. In Gene, Nov 2015
EFNB1, CYTL1 and TEX26 and TESK1, MSL1 and EVI5 in trophectoderm biopsies associated with live birth and non-implanting, respectively.
Multiple sclerosis risk loci correlate with cervical cord atrophy and may explain the course of disability.
Haghikia et al., Bochum, Germany. In Neurogenetics, Jul 2015
For nine loci-BATF, CYP27B1, IL12B, NFKB1, IL7, PLEK, EVI5, TAGAP and nrs669607-patients revealed significantly higher degree of atrophy; TYK2, RGS1 and CLEC16A revealed inverse effects.
MicroRNA-135b, a HSF1 target, promotes tumor invasion and metastasis by regulating RECK and EVI5 in hepatocellular carcinoma.
He et al., Shanghai, China. In Oncotarget, Mar 2015
The reversion-inducing-cysteine-rich protein with kazal motifs (RECK) and ecotropic viral integration site 5 (EVI5) were identified as the direct and functional targets of miR-135b in HCC.
Quantitative Proteomic Analysis of BHK-21 Cells Infected with Foot-and-Mouth Disease Virus Serotype Asia 1.
Liu et al., Lanzhou, China. In Plos One, 2014
Among these proteins, six cellular proteins, including three down-regulated (VPS28, PKR, EVI5) and three up-regulated (LYPLA1, SEC62 and DARs), were selected according to the significance of the changes and/or the relationship with PKR.
GFI1B, EVI5, MYB--additional genes that cooperate with the human BCL6 gene to promote the development of lymphomas.
Baron et al., Chicago, United States. In Blood Cells Mol Dis, 2014
We now report three newly identified cooperating genes-GFI1B, EVI5, and MYB-that we identified in the lymphomas of retroviral-injected BCL6 transgenic mice (but not in retroviral-injected non-transgenic controls); mRNA and protein expression of GFI1B and EVI5 were decreased in the murine tumors, whereas MYB mRNA and protein expression were increased or decreased.
Decoding multiple sclerosis: an update on genomics and future directions.
Oksenberg, San Francisco, United States. In Expert Rev Neurother, 2013
Follow-up experiments refined some of the association signals (IL2RA and CD58), identified gene-gene interactions (HLA-DRB1/EVI5) and revealed mechanistic insights into the functional consequences of the identified gene variants, most notably an increase in the soluble to membrane-bound ratio for IL-7, IL-2 and TNF receptors and a tyrosine-protein kinase 2-mediated immune deviation.
Proteomic analysis of fibroblastema formation in regenerating hind limbs of Xenopus laevis froglets and comparison to axolotl.
Stocum et al., Indianapolis, United States. In Bmc Dev Biol, 2013
Regenerating Xenopus limbs differed significantly from axolotl regenerating limbs in several ways: deficiency in the inositol phosphate/diacylglycerol signaling pathway, down regulation of Wnt signaling, up regulation of extracellular matrix (ECM) proteins and proteins involved in chondrocyte differentiation, lack of expression of a key cell cycle protein, ecotropic viral integration site 5 (EVI5), that blocks mitosis in the axolotl, and the expression of several patterning proteins not seen in the axolotl that may dorsalize the fibroblastema.
Mapping of the chromosomal amplification 1p21-22 in bladder cancer.
Saramäki et al., Tampere, Finland. In Bmc Res Notes, 2013
Four genes, TMED5, DR1, RPL5 and EVI5, showed significant overexpression in the SCaBER cell line compared to all the other samples tested.
Multiple sclerosis susceptibility genes: associations with relapse severity and recovery.
Waubant et al., Baltimore, United States. In Plos One, 2012
In those who were HLA-DRB1-negative, the EVI5 polymorphism was associated with attacks of less severity; in HLA-DRB1 positive patients, EVI5 was associated with attacks of greater severity and worse recovery.
Genome-wide CTCF distribution in vertebrates defines equivalent sites that aid the identification of disease-associated genes.
Gómez-Skarmeta et al., Barcelona, Spain. In Nat Struct Mol Biol, 2011
We then applied this concept to predict and functionally demonstrate that the polymorphic variants associated with multiple sclerosis located within the EVI5 gene impinge on the adjacent gene GFI1.
Isolated hepatic perfusion with high-dose melphalan results in immediate alterations in tumor gene expression in patients with metastatic ocular melanoma.
Alexander et al., Baltimore, United States. In Ann Surg Oncol, 2010
Analysis of genes showed that the Ras GTPase activator, ecotropic viral integration site 5 (EVI5), and several other melanoma-associated genes were overexpressed in pre-IHP tumors.
Tag-SNP analysis of the GFI1-EVI5-RPL5-FAM69 risk locus for multiple sclerosis.
Matesanz et al., Granada, Spain. In Eur J Hum Genet, 2010
An analysis and fine mapping of GFI-EVI5-RPL5-FAM69A locus, genotyping eight Tag-single nucleotide polymorphisms in 732 multiple sclerosis patients and 974 controls from Spain, was performed.
Stem cell exhaustion due to Runx1 deficiency is prevented by Evi5 activation in leukemogenesis.
Ito et al., Singapore, Singapore. In Blood, 2010
Stem cell exhaustion due to Runx1 deficiency is prevented by Evi5 activation in leukemogenesis.
Genome-wide association study identifies new multiple sclerosis susceptibility loci on chromosomes 12 and 20.
Australia and New Zealand Multiple Sclerosis Genetics Consortium (ANZgene), In Nat Genet, 2009
We also replicated several known MS associations (HLA-DR15, P = 7.0 x 10(-184); CD58, P = 9.6 x 10(-8); EVI5-RPL5, P = 2.5 x 10(-6); IL2RA, P = 7.4 x 10(-6); CLEC16A, P = 1.1 x 10(-4); IL7R, P = 1.3 x 10(-3); TYK2, P = 3.5 x 10(-3)) and observed a statistical interaction between SNPs in EVI5-RPL5 and HLA-DR15 (P = 0.001).
EVI5 is a risk gene for multiple sclerosis.
Hintzen et al., Rotterdam, Netherlands. In Genes Immun, 2008
EVI5 is a risk gene for multiple sclerosis.
Identification of Rab11 as a small GTPase binding protein for the Evi5 oncogene.
Eldridge et al., San Francisco, United States. In Proc Natl Acad Sci U S A, 2007
Evi5 is a Rab11 binding protein and that Evi5 may cooperate with Rab11 to coordinate vesicular trafficking, cytokinesis, and cell cycle control independent of GTPase-activating protein function
EVI5 protein associates with the INCENP-aurora B kinase-survivin chromosomal passenger complex and is involved in the completion of cytokinesis.
Cowell et al., Buffalo, United States. In Exp Cell Res, 2006
Data provide evidence that EVI5 is an essential component of the protein machinery facilitating the final stages of cell septation at the end of mitosis.
The evi5 oncogene regulates cyclin accumulation by stabilizing the anaphase-promoting complex inhibitor emi1.
Jackson et al., Stanford, United States. In Cell, 2006
The anaphase-promoting complex/cyclosome (APC/C) inhibitor Emi1 controls progression to S phase and mitosis by stabilizing key APC/C ubiquitination substrates, including cyclin A. Examining Emi1 binding proteins, we identified the Evi5 oncogene as a regulator of Emi1 accumulation.
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